In
1929 George and Mildred Burr published a paper claiming that unsaturated
fats, and specifically linoleic acid, were essential to prevent a particular
disease involving dandruff, dermatitis, slowed growth, sterility, and
fatal kidney degeneration.

In
1929, most of the B vitamins and essential trace minerals were unknown
to nutritionists. The symptoms the Burrs saw are easily produced by
deficiencies of the vitamins and minerals that they didn't know about.

What
really happens to animals when the "essential fatty acids"
are lacking, in an otherwise adequate diet?

Their
metabolic rate is very high.

Their
nutritional needs are increased.

They
are very resistant to many of the common causes of sickness and death.

They
are resistant to the biochemical and cellular changes seen in aging,
dementia, autoimmunity, and the main types of inflammation.

The
amount of polyunsaturated fatty acids often said to be essential (Holman,
1981) is approximately the amount required to significantly increase
the incidence of cancer, and very careful food selection is needed
for a diet that provides a lower amount.

When
I was studying the age pigment, lipofuscin, and its formation from polyunsaturated
fatty acids, I saw the 1927 study in which a fat free diet practically
eliminated the development of spontaneous cancers in rats (Bernstein
and Elias). I have always wondered whether George and Mildred Burr were
aware of that study in 1929, when they published their claim that polyunsaturated
fats are nutritionally essential. The German study was abstracted in
Biological Abstracts, and the Burrs later cited several studies from
German journals, and dismissively mentioned two U.S. studies* that claimed
animals could live on fat-free diets, so their neglect of such an important
claim is hard to understand. (*Their bibliography cited, without further
comment, Osborne and Mendel, 1920, and Drummond and Coward, 1921.)

Since
1927, others have demonstrated that the polyunsaturated fats are essential
for the development of cancer (and some other degenerative diseases),
but the Burrs' failed to even mention the issue at any time during their
careers. How could they, studying fat-free diets, have missed an important
contemporary publication, if I, 40 years later, saw it? There were very
few publications on dietary fats in those years, so it was hardly possible
to miss it.

When
researchers at the Clayton Foundation Biochemical Institute at the University
of Texas demonstrated that "Burr's disease" was actually a
vitamin B6 deficiency, rather than a fatty acid deficiency, the issue
was settled. Later studies failed to confirm the existence of the Burr
disease caused by a deficiency of fatty acids, though many similar conditions
were produced by a variety of other dietary defects. In 1938, a group
in Burr's own laboratory (Brown, et al.) failed to produce dermatitis
in a man during a six month experiment. Neither of the other major features
of the Burr disease, male sterility and kidney degeneration, has been
subsequently confirmed. The claim that polyunsaturated fatty acid deficiency
caused sterility of male animals ("A new and uniform cause of sterility
is shown") was quickly dropped, probably because an excess
of polyunsaturated fats was discovered to be an important cause of testicular
degeneration and sterility.

One
of the features of the Burrs' rats on the fat-free diet was that they
ate more calories and drank much more water than the rats that received
polyunsaturated fatty acids in their diet. They believed that the animals
were unable to synthesize fat without linoleic acid, although in another
context they cited a study in which the fat of rats on a fat-free diet
was similar in composition to lard: "McAmis, Anderson, and
Mendel [37] fed rats a high sucrose, fat-free diet and rendered
the fat of the entire animal. This fat had an iodine number of 64 to
71, a fairly normal value for lard."

The
"wasteful" food consumption, and the leanness of animals that
weren't fed polyunsaturated fats became fairly common knowledge by the
late 1940s, but no one repeated the Burrs' claim that the absence of
those fatty acids led quickly to the animals' death. Meanwhile, "crazy
chick disease" caused by feeding an excess of polyunsaturated fats,
and a little later, "yellow fat disease," caused by too much
fish fat, were being recognized by farmers. In the 1950s, the seed oil
industry created the anti-cholesterol diet culture, and a few decades
later, without any new "Burr-like" publications, the omega
minus 3 oils, especially fish oils, were coming to be represented as
the overlooked essential fatty acids, which were capable of preventing
the toxic effects of the original "essential" linoleic acid.

Although
the 1929 Burr paper is still often cited as proof of the essentiality
of PUFA, Burr's younger colleague (at the University of Minnesota Hormel
Institute), Ralph Holman, has cited an infant (1970), and a 78 year
old woman (in 1969), who developed dermatitis while receiving fat-free
intravenous feedings. Dermatitis, with dandruff, similar to Burr's disease,
has been produced by various nutritional deficiencies besides vitamin
B6, including a trace mineral deficiency and a biotin deficiency, so
there is no valid reason to associate dermatitis with a fat deficiency.
The cases of "EFA deficiency" produced by intravenous feedings
that have been widely cited were probably the result of a deficiency
of zinc or other trace mineral, since so-called "Total Parenteral
Nutrition" was in use for many years before the trace minerals
were added to the "total" formula. In 1975, I learned that
our local hospital was putting all premature babies on what they called
total intravenous feeding, without trace minerals, for weeks, or months.
There is still more emphasis on polyunsaturated fat in intravenous feeding
than on the essential trace nutrients.

Holman
and the Hormel Institute have been extremely influential in promoting
the doctrine of the essentiality of PUFA, including fish oils and the
omega -3 oils, but their best evidence, the Burr experiment, doesn't
make their case. Far worse than that is the effect it has had in distracting
attention from the profoundly toxic effects of the so-called essential
fatty acids. Long after he should have known better, Holman was arguing
that butter was a nutritionally inferior fat.

When
the Burrs were doing their study, Raymond Pearl was one of the most
famous biologists in the country, and his "rate of living"
theory of aging was very widely known. According to that theory, an
organism has an intrinsic potential to produce a certain total amount
of energy during its lifetime, and if it metabolizes at a higher than
normal rate, its life span will be proportionately shorter than normal.

There
is general agreement that animals on a fat free diet have a very high
metabolic rate, but the people who believe the "rate of living"
theory will be inclined to see the increased rate of metabolism as something
harmful in itself. It is clear that this is what the Burrs thought.
They didn't attempt to provide a diet that provided increased amounts
of all vitamins and minerals, in proportion to the increased metabolic
rate.

Pearl
did an experiment, sprouting cantaloupe seeds in a dish with water.
The sprouts that grew rapidly died sooner than those that grew more
slowly. They died as soon as the nutrients stored in the endosperm had
been consumed. Naturally, when nutrients are depleted, growth and metabolism
must stop. If food and air and water are rationed, then slow metabolizers
are going to live longer. But when nutritional needs are met, the organisms
with the highest metabolic rate generally are healthier and live longer.
In a study of nurses, those who habitually consumed the most calories
lived longer than those who consumed the least. Even while Pearl was
promoting his theory, other famous biologists, for example John Northrup
in Jacques Loeb's lab at the Rockefeller Institute, were making observations
that contradicted the rate of living theory. For example, around 1916,
Northrup observed that fruit flies that metabolized at the highest rate
lived the longest. Northrup was doing biology, Pearl was doing propaganda,
following Weismannism.

The
idea of extending life span by slowing metabolism and growth was a logical
implication of the "rate of living" theory of aging, and it's
an idea that is still popular. Many people have supposed that eating
less would slow metabolism. Caloric restriction does extend the life
span of many species, but it generally preserves the high metabolic
rate of youth, so that at a given age the calorie-restricted animal
has a higher rate of oxygen consumption per gram of body weight than
the unrestricted eaters.

Roy
Walford, a gerontologist who wrote about extending the human life span
to 120 years by caloric restriction, spent 30 years limiting his diet
to about 1600 calories, with little animal protein, almost no saturated
fat--fish once or twice per week, poultry or beef about once, and a
fat free milkshake for breakfast--and after about 15 years, began developing
a degenerative brain disease, ALS, one of the nerve diseases involving
lipid peroxidation and excitotoxicity. When he died from the disease,
he had lived a year longer than the normal life expectancy.

V.
Stefannson, one of the early polar explorers, spent a winter living
entirely on caribou meat, and felt that it had prevented the scurvy
that had killed so many of the other explorers, who had counted on fruit
and vegetables to prevent it. But he believed that meat was a metabolic
stimulant that made people age prematurely, as Pearl's rate of living
theory predicted. Stefannson said that Eskimo women were getting old
in their twenties, and that at the age of 60 they looked as old as Europeans
did at 80. He was a well informed anthropologist, and his observations
were probably accurate. The Eskimos he observed ate large amounts of
fish, and other unsaturated fats, and sometimes ate highly decayed fish.
An accelerated rate of aging would be expected from such a diet, because
of the toxic lipid peroxides.

Calorie-restricted
animals (on a diet of normal composition) have a lower degree of fat
unsaturation in their mitochondria as they age, preserving the relatively
more saturated fats of youth.

Birds'
mitochondrial fats are much less polyunsaturated than those of mammals,
and birds' metabolic rates are much higher, and they live much longer
than mammals of a similar size.

Over
the years, it has become evident that the polyunsaturated fats are not
very compatible with a high rate of metabolism, though they are necessary
for organisms that live at low temperatures and metabolize slowly, such
as fish and vegetables. The saturated fats solidify at low temperature;
beef fat is very stiff at refrigerator temperature, and in a fat fish,
such stiffness would be lethal.

Even
some hibernating rodents can stay alive with their body tissues close
to the freezing point, and their stored fats have to be unsaturated.
When their diet doesn't allow them to store enough polyunsaturated fat,
they fail to go into hibernation. This is probably a clue to some of
the general biological effects of the PUFA.

A
series of studies about 20 years ago showed that the functions of the
thyroid hormone are all inhibited by unsaturated fats, with the inhibition
increasing in proportion to the number of unsaturations (double bonds)
in the fat molecule.

When
the tissues are saturated with those antithyroid fats, metabolism slows,
especially when any stress, such as cold or hunger, increases the concentration
of free fatty acids in the blood stream. Stress and hypothyroidism increase
the formation of serotonin, which is an important factor in producing
the torpor of hibernation, and lowering the body temperature. The polyunsaturated
fatty acids themselves directly contribute to the formation of serotonin,
for example by increasing the ability of tryptophan to enter the brain.
In a certain cold climate, the PUFA are essential for hibernation, but
under other conditions, the rodent would be able to continue gathering
food and eating, instead of hibernating.

The
direct effects of the PUFA on the endocrine and nervous systems, as
illustrated by the hibernating squirrel, interact with their effects
on intercellular communication (including the formation of prostaglandins
and related substances), and the effects of their oxidative breakdown
products, such as acrolein. But the people who claim that they are absolutely,
rather than conditionally, essential, base their argument on the idea
that they are needed for the formation of prostaglandins and cell membranes.
The fact that cells can replicate in fat free conditions shows that
the argument from membranes is unfounded. The argument from prostaglandins
is more complex, but has no firmer foundation.

When
a dose of PUFA is administered to a lizard, which isn't a hibernator,
the lizard's body temperature is lowered by several degrees. There are
probably many ways in which the PUFA produce that effect, besides increasing
serotonin and decreasing thyroid. The PUFA are increased by estrogen,
and they increase estrogen, and have some directly estrogen-like effects.
Estrogen itself tends to lower body temperature and shift metabolism
away from oxidative energy production. Aging, like estrogen, increases
the body's content of the PUFA: Linoleic, linolenic, dihomo-gamma-linolenic,
docosahexaenoic and docosapentaenoic acids are increased by age, and
the longer chain acids increase more rapidly in women than in men (Bolton-Smith,
et al., 1997). (Women are apparently relatively protected by progesterone,
which inhibits lipolysis and prostaglandin formation, and protects the
brain, thymus, and other tissues from lipid peroxidation and other effects
of the PUFA.)

Aging
involves a decreasing metabolic rate, an increased tendency toward inflammation,
and a decreased ability to synthesize proteins. Inflammation contributes
to the decreasing ability to use oxygen, and the slowed renewal of proteins
combined with lower ability to produce energy impair the organism's
ability to control peroxidative damage and inflammation.

The
fragments of deteriorating PUFA combine with proteins and other cell
materials, producing immunogenic substances. The so-called "advanced
glycation end products," that have been blamed on glucose excess,
are mostly derived from the peroxidation of the "essential fatty
acids." The name, “glycation,” indicates the addition of sugar
groups to proteins, such as occurs in diabetes and old age, but when
tested in a controlled experiment, lipid peroxidation of polyunsaturated
fatty acids produces the protein damage about 23 times faster than the
simple sugars do (Fu, et al., 1996).

Several
autoimmune disease models in animals (involving the eye, kidney, and
pancreas) have been prevented by a deficiency of the EFA (Schreiner,
et al., 1989, Bazan, et al., 1990, Benhamou, et al., 1995).

Besides
causing a general slowing of metabolism, aging and toxic PUFA have specific
actions on the detoxifying system. The enzymes that help to detoxify
PUFA and estrogen and serotonin are inhibited by both PUFA and estrogen.
All systems, including blood vessels and the intestine, are made leaky
by estrogen and the PUFA and their products.A reduced ability to regulate the excitatory
amino acids, resulting from PUFA toxins, tends to produce excitotoxicity,
damaging nerves (Ou, et al., 2002).

Although
the interplay of the various types of nerve is very complex, a variety
of experiments suggest that the PUFA are acting directly on serotonergic
nerves, rather than just increasing the conversion of tryptophan to
serotonin.

For
example, a deficiency of the so-called essential fatty acids, EFA, makes
animals more sensitive to some anesthetics, and more resistant to others.
It makes them resistant to the anesthetics that act by promoting the
actions of serotonin, but it prolongs the effects of those that don't
act through serotonin, and these are the anesthetics such as xenon and
nitrous oxide, that apparently act by stabilizing the structure of water,
as described by Linus Pauling. Progesterone and the saturated fats seem
to act partly through the stabilizing of cell water, and estrogen and
the PUFA have opposing effects, creating cellular excitation while interfering
with the stable cellular water structure.

Serotonin
interferes with slow wave sleep, and promotes cortisol, both of which
can be harmful to brain cells. (Hypothyroidism is one of the causes
of a decrease in slow wave sleep.) Babies whose mothers' serum contained
more DHA were more wakeful on their second day of life, than the babies
of low-DHA mothers. The amide of oleic acid is a sleep promoter, with
apparent antiserotonin activity (Yang, et al., 2003), and since oleic
acid tends to be displaced by diets high in PUFA, this suggests another
way in which the highly unsaturated fatty acids could promote serotonin's
effects.

People
who don't have a normal amount of slow wave sleep are likely to have
slow reaction times when they are awake, and quickness of reactions
is a good indicator of general intelligence.

Manufacturers
of baby formulas are claiming that the highly unsaturated fatty acids
accelerate brain development, but they neglect to mention studies that
show either no effect, or retardation of development. In some of the
tests that are used to measure infant development, a generalized state
of arousal or anxiety could be interpreted as "more mature."

In
one experiment, animals that received less than 0.32% of their calories
as EFA grew slightly less than rats on a standard diet, but their brains
were as large as those of normal rats (Bruckner, et al., 1984). That
is, their brain to body ratio was a little larger than normal, which
is a typical feature of individuals with a higher metabolic rate. That
result is very different from the claims of the baby food industry,
that the brain is the organ most easily damaged by a PUFA deficiency.

One
of the standard signs of toxicity is the enlargement of the spleen and
liver, and that effect is produced by larger amounts of the EFA. The
weight of the thymus is reduced by PUFA in the diet (Guimarães, et
al., 1990). Thymus cells tend to be easily killed by a combination of
stress and EFA, and bone marrow cells, though less sensitive than thymic
cells, are damaged by lipid peroxidation of the PUFA. The effects of
PUFA on the thymus were compared to those of radiation by Soviet researchers.
Immunodeficiency, produced largely by damage to thymic cells, increases
when larger amounts of PUFA are eaten for a prolonged time.

The
growth and metastasis of a variety of tumors are inhibited by saturated
fatty acids, and increased by fish oil--as much as 10 times in number
of metastases, 1000 times in size (Griffini, et al., 1998).

Mothers
whose breast milk contains more long-chain n-3 fatty acids are more
likely to have allergic children (Stoney, et al., 2004). (And children
whose mothers are allergic have higher levels of DHA and EPA in their
tissues.) These associations aren't mentioned by the manufacturers who
speak of those fats as essential.

When
animals have been "deprived" of the EFA during gestation and
nursing, and then given a standard diet, they develop larger bones,
with a thicker cortex and more trabecular bone, both of which would
suggest a lower level of stress. Many types of inflammation and stress
are significantly reduced in "EFA deficient" animals. Inflammation
caused by the injection of carrageenan is decreased, partly because
of the absence of prostaglandins in these animals. The absence of the
EFA protects against colitis and nephritis ( ). The kidneys are more
effective in several ways in the deficient animals.

Shock,
caused by the injection of endotoxin, which is 100% lethal to normally
fed animals, is only 24% lethal to the deficient animals.

Poisons
are much less harmful to deficient animals, for example, a cobra venom
factor causes less tissue damage to their lungs.

Concussive
trauma and burns cause much less damage to deficient animals.

The
endothelial lining of blood vessels is protected by saturated fats and
oleic acid, damaged by polyunsaturated, and their barrier function is
improved by the absence of PUFA.

The
lesions of atherosclerosis and cataracts contain some of the same oxidized
lipids as the age pigment itself. When large deposits of age pigment
become visible, it's probably because the general reduction of metabolism
and protein synthesis has interfered with the normal processes for removing
debris. The age pigment contributes to degeneration by wasting energy
and oxygen, weakening the antioxidation, antiglycation, and other defensive
systems.

The
EFA amplify nearly all kinds of injury and stress, and the results of
many recent publications make it look as though serotonin interacts
harmfully with the EFA in most of these situations. The specific balance
of polyunsaturated fatty acids, and their various breakdown products,
from carbon monoxide, glyoxal, and acrolein, to the larger aldehydes
and radicals, and the stress-induced substances such as serotonin, histamine,
estrogens, can produce an immense variety of biological problems.

When
the various claims of an EFA "deficiency disease" or syndrome
or symptom are examined, their inconsistency over the years makes skepticism
seem increasingly justified. The Burrs' publications were typical of
others, in failing to describe and account for the evidence that contradicted
their claims. Claiming that certain fatty acids are essential, a scientific
approach would require showing what was wrong with the experiments that
showed that they were not essential, and especially, those that showed
that they were positively harmful.

In
this culture that repeatedly makes such claims of essentiality, the
growing number of reports of biological superiority of "deficient"
animals suggests that nutritional research may be near the point at
which it can resume the line of study begun by Northrup, Osborne, Mendel,
Drummond, Bernstein, Elias, and others, that was interrupted for 60
years by industrial interests that promoted antiscientific opinions.

For
example, in 1914 F.P. Rous showed that limiting food intake reduced
the incidence of cancer, and then in 1915 and 1917, Osborne and Mendel
showed that food restriction extended the fertility and longevity of
female rats. The association between estrogen and cancer had become
known during this time, and vitamin E, which was originally known as
the fertility vitamin, was soon recognized to have antiestrogenic properties,
as well as to prevent the deadly effects of excessive polyunsaturated
fats in the diet. My endocrinology professor, A.S. Soderwall, who had
found that excess estrogen prevented (or interrupted) pregnancy, demonstrated
that increased vitamin E extended fertility in aging female rodents.

By
the time I began my research, it seemed clear that it had been the reduction
of PUFA in the diet which, like the addition of vitamin E, had prevented
sterility in the calorie restriction experiments, and that those treatments
had limited the effects of estrogen in the aging organisms.

Estrogen,
by activating phospholipase A2, acts to amplify the toxic effects of
PUFA in the tissues, and these effects increase with age, and with decreased
amounts of thyroid and progesterone.

Antioxidants
can slightly retard the cumulative degenerative effects of the fats
interacting with estrogen, serotonin, and other mediators of inflammation,
but real elimination of the degenerative diseases will require an exploration
of the effects of the entire series of lipid signalling substances derived
from the saturated and omega minus 9 fatty acids.

J.
Biol. Chem. 82:345-367.(1929) A new deficiency disease produced by
the rigid exclusion of fat from the diet. Burr, G. & Burr, M.

J.
Biol. Chem. 86:587-621. (1930) On the nature and role of the fatty
acids essential in nutrition. Burr, G. & Burr, M.

J
Natl Cancer Inst. 1984 Jul;73(1):185-91. Dietary lipid effects on
the growth, membrane composition, and prolactin-binding capacity of
rat mammary tumors. Cave WT Jr, Jurkowski JJ. "Our results
indicated that 1) when the polyunsaturated lipid component (corn oil)
of the diet exceeded 3%, it was the quantitative level of total lipid,
rather than the level of polyunsaturated lipid alone, that best correlated
with the observed reduction in tumor latent period; 2) when the polyunsaturated
lipid content of the diet fell below 3%, there was a decrease in tumor
incidence and an increase in the mean latent period...."

Lipids.
1997 Sep;32(9):979-88. Modulation of adjuvant-induced arthritis by
dietary arachidonic acid in essential fatty acid-deficient rats.
Chinn KS, Welsch DJ, Salsgiver WJ, Mehta A, Raz A, Obukowicz MG. "Controlled
feeding of linoleic acid (LA) or arachidonic acid (AA) to essential
fatty acid-deficient (EFAD) rats was used to define the relationship
between dietary AA and the inflammatory response evoked during adjuvant-induced
arthritis.""Compared to rats fed the standard laboratory
chow diet (Control), edema in the primary hind footpads was decreased
by 87% in EFAD, 71% in EFAD + 1x AA, 45% in EFAD + 10x AA, and 30% in
EFAD + 0.5x LA. The decrease in edema in the footpads of EFAD rats was
nearly identical to the decrease in edema in the footpads of Control
rats dosed with indomethacin.
Hind footpad edema correlated with the final AA plasma level and eicosanoid
levels extracted from hind footpad tissue, but not with neutrophil infiltration."

J
Nutr. 1981 Nov;111(11):2039-43. Effects of dietary fatty acids on
delayed-type hypersensitivity in mice. Dewille JW, Fraker PJ, Romsos
DR. Effects of an essential fatty acid deficient (EFAD) [0% corn oil
(CO)] diet and a diet high in polyunsaturated fatty acids [PUFA (50%
CO)] on one aspect of in vivo T cell function [delayed-type hypersensitivity
(DTH)] were assessed. After a 70-day feeding trial, DTH was reduced
by 30% in mice fed the EFAD diet, but the response of mice fed the
high PUFA diet equaled that of control mice fed a diet containing 13%
CO. The time required for the EFAD diet to reduce DTH was 42 days.
Although consumption of the EFAD diet reduced DTH, this reduction
was rapidly reversed, within 7 days, by switching the EFAD mice to the
control diet. These results indicate that :1) consumption of the EFAD
diet reduces one aspect of in vivo T cell function (DTH), but the effect
can be reversed by refeeding the control diet; and 2) a high PUFA diet
does not adversely affect DTH.

Biochim
Biophys Acta. 2005 Jan 5;1686 3:248-54. Perinatal essential fatty
acid deficiency influences body weight and bone parameters in adult
male rats. Korotkova M, Ohlsson C, Gabrielsson B, Hanson LA, Strandvik
B. Department of Pediatrics, Goteborg University, The Queen Silvia Children's
Hospital, SE 41685 Goteborg, Sweden. Marina.Korotkova@cmm.ki.se Fetal
and postnatal nutrition have long-term effects on the risk for development
of diseases late in life in humans and animals. The aim of the present
study was to investigate the effect of dietary deficiency of essential
fatty acids (EFA) in the perinatal period on later body weight and bone
mass. During late gestation
and throughout lactation, rats were fed a control or an EFA-deficient
(EFAD) diet. At 3 weeks of age the offspring were weaned onto an ordinary
chow and followed until adult age. The mean body weight of adult rats
receiving the EFAD diet during the perinatal period was significantly
increased from 12 weeks of age compared to the controls (P<0.05).
Analysis by peripheral quantitative computerized tomography (pQCT) at
44 weeks of age showed that the trabecular volumetric bone mineral density
(BMD) of the femur was significantly decreased (P<0.05) but the
cortical bone mineral content, cortical area, and cortical thickness
were increased (P<0.05) in the EFAD group of rats. The length
of the femur was not affected. In conclusion, neonatal EFA deficiency
was in adult rats associated with increased body weight and significant
changes in both cortical and trabecular bone. The results indicate that
regulatory mechanisms related to bone mass seemed to be programmed by
EFA in the perinatal period. The nature of this modulation needs
to be identified.

Neurobiol Aging. 1982 Fall;3(3):173-8. Lipid peroxides in brain during
aging and vitamin E deficiency: possible relations to changes in neurotransmitter
indices. Noda Y, McGeer PL, McGeer EG. "Lipid peroxide levels,
were found to be significantly higher in brains of 18 month old as compared
to 4 month old rats, with particularly large increases occurring
in the olfactory bulb, globus pallidus, cerebral cortex and caudate-putamen
(CP). Eighteen month old rats fed a vitamin E deficient diet for
9 months before sacrifice had lipid peroxide levels significantly higher
than age-matched controls in the cerebral cortex, hippocampus and
hypothalamus." "Age-related decreases were seen in choline
acetyltransferase, acetylcholinesterase and 3H-QNB binding in some but
not all brain regions, while GABA transaminase and MAO showed age-related
increases." "As compared with controls, vitamin E deficient
rats showed decreases of 38% in cortical 3H-DHA binding, of 33% in 3H-QNB
binding in the CP and of 23% and 12% in choline acetyltransferase in
the CP and cerebellum, respectively."

Surg
Today. 2003;33(8):600-5. Beneficial effects of n-9 eicosatrienoic
acid on experimental bowel lesions. Yoshida H, Soh H, Sando K, Wasa
M, Takagi Y, Okada A. PURPOSE: Dietary fortification of n-9 polyunsaturated
fatty acids (PUFA) or 5,8,11-eicosatrienoic acid (ETrA) as well as n-3
PUFA might contribute to the suppression of leukotriene B4 (LTB4) synthesis
and thereby reduce inflammatory bowel lesions. As a result, the effect
of an ETrA-enriched diet on experimental bowel lesions was examined
in this study. METHODS: In Expt. 1, rats were freely fed either an ETrA-enriched
or a standard diet. After 7 days of feeding, acute bowel lesions were
induced by the subcutaneous injection of 10 mg/kg indomethacin. In Expt.
2, chronic bowel lesions were made by performing subcutaneous injections
of 7.5 mg/kg indomethacin twice. After the first injection, the rats
were freely fed either an ETrA-enriched or a standard diet for 7 days.
RESULTS: In both experiments, the rats fed an ETrA-enriched diet showed
increased levels of ETrA in the plasma and intestinal mucosa, and a
decreased inflammation score. However, there was no significant decrease
in plasma and intestinal mucosal LTB4 in the ETrA-enriched diet-fed
rats. CONCLUSION: These results suggest that the dietary supplementation
of ETrA may have both prophylactic and therapeutic effects on experimentally
produced bowel lesions. Further investigations are necessary to clarify
the effects of ETrA on bowel lesions and its mechanisms.